Comparison of treatments for mild secondary hyperparathyroidism in hemodialysis patients

O. S. Indridason, Leigh Quarles

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

Background. In the management of patients with mild secondary hyperparathyroidism, it is not known whether calcium supplementation alone is sufficient to correct abnormalities in bone and mineral metabolism or if calcitriol is needed in either physiologic oral or intravenous pharmacologic doses. Methods. This was a 40-week prospective nonmasked trial of 52 patients [parathyroid hormone (PTH) 150 to 600 pg/mL] who were randomized to receive escalating doses of either calcium carbonate (CaCO3) alone (calcium group, N = 11), daily oral calcitriol (oral group, N = 20), or intermittent intravenous calcitriol (IV group, N = 21). The groups were compared with regard to changes in serum intact PTH, serum bone-specific alkaline phosphatase (BAP), incidence of hypercalcemia (>10.5 mg/dL), and hyperphosphatemia (>6.5 mg/dL). Results. PTH levels decreased in all groups (P < 0.01, paired t-test). In the calcium group, PTH (mean ± SEM) decreased from 325 ± 46.2 to 160 ± 44.5 pg/mL. In the oral group, it decreased from 265 ± 26.4 to 125 ± 23.7 pg/mL, and in the IV group, it decreased from 240 ± 27.7 to 65 ± 10.0 pg/mL. Upon analysis of covariance, controlling for the initial PTH level, we found no differences in the PTH response between the groups (P > 0.10). In contrast, the BAP concentration increased from 20.7 ± 7.6 to 27.5 ± 7.0 μg/L in the calcium group (P = 0.17), decreased from 20.6 ± 3.9 to 17.8 ± 4.5 μg/L in the oral group (P = 0.26), and from 19.1 ± 2.6 to 10.6 ± 1.1 μg/L in the IV group (P = 0.007). Serum calcium increased significantly in all groups from 8.4 ± 0.25 to 9.0 ± 0.28, 8.5 ± 0.16 to 9.2 ± 0.27, and 8.7 ± 0.16 to 9.4 ± 0.18 mg/dL in the calcium, oral, and IV groups, respectively (P = NS difference between groups). Serum phosphorus was significantly lower in the calcium group throughout the study (P = 0.02). Hypercalcemic episodes were 2.0 ± 0.8, 3.0 ± 0.6, and 3.4 ± 0.6 per patient-year (P > 0.10), and hyperphosphatemic episodes were 0.9 ± 0.56, 4.2 ± 0.79 and 4.9 ± 0.84 in the calcium, oral, and IV groups, respectively (P < 0.01). Conclusion. In mild secondary hyperparathyroidism, all three strategies are effective. High-dose CaCO3 alone may be sufficient to control PTH with a favorable side-effect profile, but calcitriol appears to have additional suppressive effects on bone that are greater following the intravenous route of administration and may increase the risk of adynamic bone disease.

Original languageEnglish (US)
Pages (from-to)282-292
Number of pages11
JournalKidney International
Volume57
Issue number1
DOIs
StatePublished - Jan 1 2000

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Secondary Hyperparathyroidism
Renal Dialysis
Calcium
Calcitriol
Parathyroid Hormone
Bone and Bones
Serum
Therapeutics
Alkaline Phosphatase
Hyperphosphatemia
Calcium Carbonate
Bone Diseases
Hypercalcemia
Intravenous Administration
Phosphorus
Minerals
Incidence

All Science Journal Classification (ASJC) codes

  • Nephrology

Cite this

Comparison of treatments for mild secondary hyperparathyroidism in hemodialysis patients. / Indridason, O. S.; Quarles, Leigh.

In: Kidney International, Vol. 57, No. 1, 01.01.2000, p. 282-292.

Research output: Contribution to journalArticle

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abstract = "Background. In the management of patients with mild secondary hyperparathyroidism, it is not known whether calcium supplementation alone is sufficient to correct abnormalities in bone and mineral metabolism or if calcitriol is needed in either physiologic oral or intravenous pharmacologic doses. Methods. This was a 40-week prospective nonmasked trial of 52 patients [parathyroid hormone (PTH) 150 to 600 pg/mL] who were randomized to receive escalating doses of either calcium carbonate (CaCO3) alone (calcium group, N = 11), daily oral calcitriol (oral group, N = 20), or intermittent intravenous calcitriol (IV group, N = 21). The groups were compared with regard to changes in serum intact PTH, serum bone-specific alkaline phosphatase (BAP), incidence of hypercalcemia (>10.5 mg/dL), and hyperphosphatemia (>6.5 mg/dL). Results. PTH levels decreased in all groups (P < 0.01, paired t-test). In the calcium group, PTH (mean ± SEM) decreased from 325 ± 46.2 to 160 ± 44.5 pg/mL. In the oral group, it decreased from 265 ± 26.4 to 125 ± 23.7 pg/mL, and in the IV group, it decreased from 240 ± 27.7 to 65 ± 10.0 pg/mL. Upon analysis of covariance, controlling for the initial PTH level, we found no differences in the PTH response between the groups (P > 0.10). In contrast, the BAP concentration increased from 20.7 ± 7.6 to 27.5 ± 7.0 μg/L in the calcium group (P = 0.17), decreased from 20.6 ± 3.9 to 17.8 ± 4.5 μg/L in the oral group (P = 0.26), and from 19.1 ± 2.6 to 10.6 ± 1.1 μg/L in the IV group (P = 0.007). Serum calcium increased significantly in all groups from 8.4 ± 0.25 to 9.0 ± 0.28, 8.5 ± 0.16 to 9.2 ± 0.27, and 8.7 ± 0.16 to 9.4 ± 0.18 mg/dL in the calcium, oral, and IV groups, respectively (P = NS difference between groups). Serum phosphorus was significantly lower in the calcium group throughout the study (P = 0.02). Hypercalcemic episodes were 2.0 ± 0.8, 3.0 ± 0.6, and 3.4 ± 0.6 per patient-year (P > 0.10), and hyperphosphatemic episodes were 0.9 ± 0.56, 4.2 ± 0.79 and 4.9 ± 0.84 in the calcium, oral, and IV groups, respectively (P < 0.01). Conclusion. In mild secondary hyperparathyroidism, all three strategies are effective. High-dose CaCO3 alone may be sufficient to control PTH with a favorable side-effect profile, but calcitriol appears to have additional suppressive effects on bone that are greater following the intravenous route of administration and may increase the risk of adynamic bone disease.",
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N2 - Background. In the management of patients with mild secondary hyperparathyroidism, it is not known whether calcium supplementation alone is sufficient to correct abnormalities in bone and mineral metabolism or if calcitriol is needed in either physiologic oral or intravenous pharmacologic doses. Methods. This was a 40-week prospective nonmasked trial of 52 patients [parathyroid hormone (PTH) 150 to 600 pg/mL] who were randomized to receive escalating doses of either calcium carbonate (CaCO3) alone (calcium group, N = 11), daily oral calcitriol (oral group, N = 20), or intermittent intravenous calcitriol (IV group, N = 21). The groups were compared with regard to changes in serum intact PTH, serum bone-specific alkaline phosphatase (BAP), incidence of hypercalcemia (>10.5 mg/dL), and hyperphosphatemia (>6.5 mg/dL). Results. PTH levels decreased in all groups (P < 0.01, paired t-test). In the calcium group, PTH (mean ± SEM) decreased from 325 ± 46.2 to 160 ± 44.5 pg/mL. In the oral group, it decreased from 265 ± 26.4 to 125 ± 23.7 pg/mL, and in the IV group, it decreased from 240 ± 27.7 to 65 ± 10.0 pg/mL. Upon analysis of covariance, controlling for the initial PTH level, we found no differences in the PTH response between the groups (P > 0.10). In contrast, the BAP concentration increased from 20.7 ± 7.6 to 27.5 ± 7.0 μg/L in the calcium group (P = 0.17), decreased from 20.6 ± 3.9 to 17.8 ± 4.5 μg/L in the oral group (P = 0.26), and from 19.1 ± 2.6 to 10.6 ± 1.1 μg/L in the IV group (P = 0.007). Serum calcium increased significantly in all groups from 8.4 ± 0.25 to 9.0 ± 0.28, 8.5 ± 0.16 to 9.2 ± 0.27, and 8.7 ± 0.16 to 9.4 ± 0.18 mg/dL in the calcium, oral, and IV groups, respectively (P = NS difference between groups). Serum phosphorus was significantly lower in the calcium group throughout the study (P = 0.02). Hypercalcemic episodes were 2.0 ± 0.8, 3.0 ± 0.6, and 3.4 ± 0.6 per patient-year (P > 0.10), and hyperphosphatemic episodes were 0.9 ± 0.56, 4.2 ± 0.79 and 4.9 ± 0.84 in the calcium, oral, and IV groups, respectively (P < 0.01). Conclusion. In mild secondary hyperparathyroidism, all three strategies are effective. High-dose CaCO3 alone may be sufficient to control PTH with a favorable side-effect profile, but calcitriol appears to have additional suppressive effects on bone that are greater following the intravenous route of administration and may increase the risk of adynamic bone disease.

AB - Background. In the management of patients with mild secondary hyperparathyroidism, it is not known whether calcium supplementation alone is sufficient to correct abnormalities in bone and mineral metabolism or if calcitriol is needed in either physiologic oral or intravenous pharmacologic doses. Methods. This was a 40-week prospective nonmasked trial of 52 patients [parathyroid hormone (PTH) 150 to 600 pg/mL] who were randomized to receive escalating doses of either calcium carbonate (CaCO3) alone (calcium group, N = 11), daily oral calcitriol (oral group, N = 20), or intermittent intravenous calcitriol (IV group, N = 21). The groups were compared with regard to changes in serum intact PTH, serum bone-specific alkaline phosphatase (BAP), incidence of hypercalcemia (>10.5 mg/dL), and hyperphosphatemia (>6.5 mg/dL). Results. PTH levels decreased in all groups (P < 0.01, paired t-test). In the calcium group, PTH (mean ± SEM) decreased from 325 ± 46.2 to 160 ± 44.5 pg/mL. In the oral group, it decreased from 265 ± 26.4 to 125 ± 23.7 pg/mL, and in the IV group, it decreased from 240 ± 27.7 to 65 ± 10.0 pg/mL. Upon analysis of covariance, controlling for the initial PTH level, we found no differences in the PTH response between the groups (P > 0.10). In contrast, the BAP concentration increased from 20.7 ± 7.6 to 27.5 ± 7.0 μg/L in the calcium group (P = 0.17), decreased from 20.6 ± 3.9 to 17.8 ± 4.5 μg/L in the oral group (P = 0.26), and from 19.1 ± 2.6 to 10.6 ± 1.1 μg/L in the IV group (P = 0.007). Serum calcium increased significantly in all groups from 8.4 ± 0.25 to 9.0 ± 0.28, 8.5 ± 0.16 to 9.2 ± 0.27, and 8.7 ± 0.16 to 9.4 ± 0.18 mg/dL in the calcium, oral, and IV groups, respectively (P = NS difference between groups). Serum phosphorus was significantly lower in the calcium group throughout the study (P = 0.02). Hypercalcemic episodes were 2.0 ± 0.8, 3.0 ± 0.6, and 3.4 ± 0.6 per patient-year (P > 0.10), and hyperphosphatemic episodes were 0.9 ± 0.56, 4.2 ± 0.79 and 4.9 ± 0.84 in the calcium, oral, and IV groups, respectively (P < 0.01). Conclusion. In mild secondary hyperparathyroidism, all three strategies are effective. High-dose CaCO3 alone may be sufficient to control PTH with a favorable side-effect profile, but calcitriol appears to have additional suppressive effects on bone that are greater following the intravenous route of administration and may increase the risk of adynamic bone disease.

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